Low total haemoglobin mass, blood volume and aerobic capacity in men with type 1 diabetes

Blood O₂ carrying capacity affects aerobic capacity (VO_2max). Patients with type 1 diabetes have a risk for anaemia along with renal impairment, and they often have low VO_2max. We investigated whether total haemoglobin mass (tHb-mass) and blood volume (BV) differ in men with type 1 diabetes (T1D, n = 12) presently without complications and in healthy men (CON, n = 23) (age-, anthropometry-, physical activity-matched), to seek an explanation for low VO_2max. We determined tHb-mass, BV, haemoglobin concentration ([Hb]), and VO_2max in T1D and CON. With similar (mean ± SD) [Hb] (144 vs. 145 g l^?1), T1D had lower tHb-mass (10.1 ± 1.4 vs. 11.0 ± 1.1 g kg^?1, P < 0.05), BV (76.8 ± 9.5 vs. 83.5 ± 8.3 ml kg^?1, P < 0.05) and VO_2max (35.4 ± 4.8 vs. 44.9 ± 7.5 ml kg^?1 min^?1, P < 0.001) than CON. VO_2max correlated with tHb-mass and BV both in T1D (r = 0.71, P < 0.01 and 0.67, P < 0.05, respectively) and CON (r = 0.54, P < 0.01 and 0.66, P < 0.001, respectively), but not with [Hb]. Linear regression slopes were shallower in T1D than CON both between VO_2max and tHb-mass (2.4 and 3.6 ml kg^?1 min^?1 vs. g kg^?1, respectively) and VO_2max and BV (0.3 and 0.6 ml kg^?1 min^?1 vs. g kg^?1, respectively), indicating that T1D were unable to reach similar VO_2max than CON at a given tHb-mass and BV. In conclusion, low tHb-mass and BV partly explained low VO_2max in T1D and may provide early and more sensitive markers of blood O₂ carrying capacity than [Hb] alone.     

Type A and B monoamine oxidase activities in the human and rat kidney

The present work has examined the distribution of the two isoforms of monoamine oxidase (MAO), type MAO-A and MAO-B, in the cortex and medulla of the human and rat kidney. Homogenates of renal cortex and renal medulla were prepared in 67 mmoles 1^-1phosphate buffer (pH = 7.2) and MAO activity was determined with [³H]5-hydroxytryptamine ([³H]5HT) and [¹⁴C]β-phenylethylamine ([¹⁴C]β-PEA) as preferential substrates of type A and type B MAO, respectively. K_m and V_max values for the two substrates were also calculated. Both MAO-A and MAO-B are present in the cortex and the medulla of the human and rat kidneys. In the human kidney, MAO-A activity was found to be similar in the cortex (V_max= 142.70±45.05 nmoles mg^-1protein h^-1) and medulla (V_max= 133.91±35.51 nmoles mg^-1protein h^-1); MAO-B activity was found to be higher in the cortex (V_max= 166.19±19.75 nmoles mg¹protein h^-1) than in the medulla (V_max= 92.91±13.22 nmoles mg^-1protein h^-1). In the rat kidney, MAO-A was also found to be similar in the cortex (V_max= 62.35±1.74 nmoles mg^-1protein h^-1) and the medulla (V_max= 59.42±0.97 nmoles mg^-1protein h^-1) and higher than the activity of MAO-B in the two renal areas (cortex, V_max= 31.06±1.09 nmoles mg^-1protein h^-1; medulla, V_max= 14.93±0.97 nmoles mg^-1protein h^-1). No statistically significant differences were found between the K_m values towards [³H]5HT and [¹⁴C]β-PEA in the cortex and the medulla of the human and rat kidneys. The results show that in both renal areas, activity of the enzyme is higher in the human kidney than in the rat kidney. Furthermore, in the human kidney, in contrast with the rat kidney, MAO-B activity closely follows MAO-A activity.     

Glucose kinetics during exercise in trained men

Six trained men were studied to examine the relative increases in hepatic glucose output and peripheral glucose uptake during 40 min of exercise at 75%Vo_2max. Rates of appearance (Ra) and disappearance (Rd) were measured using a primed, continuous intravenous infusion of D-[3-³H]glucose. Plasma glucose increased (P < 0.05) from 4.8 ± 0.2 mmol I^-1 at rest to 6.2 ± 0.5 mmol l^-1 after 40 min of exercise. Both Ra and Rd increased (P < 0.05) during exercise, however, during the early phase of exercise, Ra exceeded Rd (P < 0.05). Ra peaked at 42.0 ±3.2/tmol kgf¹ min^-1 after approximately 15 min of exercise. In contrast, the highest Rd of 33.9 ± 4.3 μmol kg^-1 min^-1 was measured at the end of exercise. In additional experiments, five men were studied during 40 min of exercise at 70–75%Vo_2max, 2 h after ingestion of the non-selective β-adrenergic antagonist timolol or a placebo capsule. Subjects were unable to complete the exercise bout following timolol, fatiguing after 28.0 ± 4.0 min (P < 0.05). The increase in blood glucose from 4.3 ±0.1 to 4.7 ± 0.3 mmol l^-1 (P < 0.05) following 20 min of exercise under control conditions was completely abolished by prior timolol ingestion (4.2 ± 0.2 to 4.1±0.2 mmol l^-1). These results demonstrate that during exercise at 75%Vo_2max in trained men, hepatic glucose output is not always closely matched to peripheral muscle glucose uptake and may be subject to feed-forward regulation. The abolition of the hyperglycaemia with non-selective β-adrenergic blockade implicates adrenaline in this response.     

Local and systemic effects on blood lactate concentration during exercise with small and large muscle groups

To evaluate the relationship between lactate release and [lac]_art and to investigate the influence of the catecholamines on the lactate release, 14 healthy men [age 25±3 (SE) year] were studied by superimposing cycle on forearm exercise, both at 65% of their maximal power reached in respective incremental tests. Handgrip exercise was performed for 30 min at 65% of peak power. In addition, between the tenth and the 22nd minute, cycling with the same intensity was superimposed. The increase in venous lactate concentration ([lac]_ven) (rest: 1.3±0.4 mmol·l⁻¹; 3rd min: 3.9±0.8 mmol·l⁻¹) begins with the forearm exercise, whereas arterial lactate concentration ([lac]_art) remains almost unchanged. Once cycling has been added to forearm exercise (COMB), [lac]_art increases with a concomitant increase in [lac]_ven (12th min: [lac]_art, 3.2±1.3 mmol·l⁻¹; [lac]_ven, 5.7±2.2 mmol·l⁻¹). A correlation between oxygen tension (P_vO₂) and [lac]_ven cannot be detected. There is a significant correlation between [lac]_art and norepinephrine ([NE]) (y=0.25x+1.2; r=0.815; p<0.01) but no correlation between lactate release and epinephrine ([EPI]) at moderate intensity. Our main conclusion is that lactate release from exercising muscles at moderate intensities is neither dependent on P_vO₂ nor on [EPI] in the blood.     

Lung oxidative stress as related to exercise and altitude. Lipid peroxidation evidence in exhaled breath condensate: a possible predictor of acute mountain sickness

Lung oxidative stress (OS) was explored in resting and in exercising subjects exposed to moderate and high altitude. Exhaled breath condensate (EBC) was collected under field conditions in male high-competition mountain bikers performing a maximal cycloergometric exercise at 670 m and at 2,160 m, as well as, in male soldiers climbing up to 6,125 m in Northern Chile. Malondialdehyde concentration [MDA] was measured by high-performance liquid chromatography in EBC and in serum samples. Hydrogen peroxide concentration [H₂O₂] was analysed in EBC according to the spectrophotometric FOX₂ assay. [MDA] in EBC of bikers did not change while exercising at 670 m, but increased from 30.0±8.0 to 50.0±11.0 nmol l⁻¹ (P<0.05) at 2,160 m. Concomitantly, [MDA] in serum and [H₂O₂] in EBC remained constant. On the other hand, in mountaineering soldiers, [H₂O₂] in EBC under resting conditions increased from 0.30±0.12 μmol l⁻¹ at 670 m to 1.14±0.29 μmol l⁻¹ immediately on return from the mountain. Three days later, [H₂O₂] in EBC (0.93 ±0.23 μmol l⁻¹) continued to be elevated (P<0.05). [MDA] in EBC increased from 71±16 nmol l⁻¹ at 670 m to 128±26 nmol l⁻¹ at 3,000 m (P<0.05). Changes of [H₂O₂] in EBC while ascending from 670 m up to 3,000 m inversely correlated with concomitant variations in HbO2 saturation (r=−0.48, P<0.05). AMS score evaluated at 5,000 m directly correlated with changes of [MDA] in EBC occurring while the subjects moved from 670 to 3,000 m (r=0.51, P<0.05). Lung OS may constitute a pathogenic factor in AMS.     

Attenuated relationship between cardiac output and oxygen uptake during high-intensity exercise

Aim: Recent findings have challenged the belief that the cardiac output (CO) and oxygen consumption (VO₂) relationship is linear from rest to maximal exercise. The purpose of this study was to determine the CO and stroke volume (SV) response to a range of exercise intensities, 40–100% of VO_2max, during cycling. Methods: Ten well‐trained cyclists performed a series of discontinuous exercise bouts to determine the CO and SV vs. VO₂ responses. Results: The rate of increase in CO, relative to VO₂, during exercise from 40 to 70% of VO_2max was 4.4 ± 1.4 L L^?1. During exercise at 70–100% of VO_2max, the rate of increase in CO was reduced to 2.1 ± 0.9 L L^?1 (P = 0.01). Stroke volume during exercise at 80–100% of VO_2max was reduced by 7% when compared to exercise at 50–70% of VO_2max (134 ± 5 vs. 143 ± 5 mL per beat, P = 0.02). Whole body arterial‐venous O₂ difference increased significantly as intensity increased. Conclusion: The observation that the rate of increase in CO is reduced as exercise intensity increases suggests that cardiovascular performance displays signs of compromised function before maximal VO₂ is reached.     

The effects of 24 weeks of moderate- or high-intensity exercise on insulin resistance

This study was designed to investigate the effect of exercise intensity on insulin resistance by comparing moderate- and high-intensity interventions of equal energy cost. Maximum oxygen consumption (VO_2max), insulin, glucose and triglycerides were measured in 64 sedentary men before random allocation to a non-exercise control group, a moderate-intensity exercise group (three 400-kcal sessions per week at 60% of VO_2max) or a high-intensity exercise group (three 400-kcal sessions per week at 80% of VO_2max). An insulin sensitivity score was derived from fasting concentrations of insulin and triglycerides, and insulin resistance was assessed using the homeostasis model assessment of insulin resistance (HOMA-IR). Data were available for 36 men who finished the study. After 24 weeks, insulin concentration decreased by 2.54±4.09 and 2.37±3.35 mU l⁻¹, insulin sensitivity score increased by 0.91±1.52 and 0.79±1.37, and HOMA-IR decreased by −0.6±0.8 and −0.5±0.8 in the moderate- and high-intensity exercise groups, respectively. When data from the exercise groups were combined, one-way analysis of variance with one-tailed post hoc comparisons indicated that these changes were significantly greater than those observed in the control group (all P<0.05). Twenty-four week changes in insulin concentration, insulin sensitivity score and HOMA-IR were not significantly different between the exercise groups. These data suggest that exercise training is accompanied by a significant reduction in insulin resistance, as indicated by well-validated surrogate measures. These data also suggest that moderate-intensity exercise is as effective as high-intensity exercise when 400 kcal are expended per session.     

Power and peak blood lactate at 5050 m with 10 and 30 s ‘all out’ cycling

Anecdotal observations suggest that the reduction in peak lactate accumulation in blood ([La]_{b peak}) after exhausting exercise, in chronic hypoxia vs. normoxia, may be related to the duration of the exercise protocol, being less pronounced after short supramaximal exercise than after incremental exercise (IE) lasting several minutes. To test this hypothesis, six healthy male Caucasians (age 36.8 ± 7.3, x¯ ± SD) underwent three exercise protocols on a cycle ergometer, at sea level (SL) and after 21 ± 10 days at 5050 m altitude (ALT): (1) 10 s, (2) 30 s ‘all out’ exercise and (3) IE leading to exhaustion in ～20–25 min. ‘Average’ power output (p¯) was calculated for 10 or 30 s ‘all out’; maximal power output (P_max) was determined for IE. Lactate concentration in arterialized capillary blood ([La]_b) was measured at rest and at different times during recovery; the highest [La]_b during recovery was taken as [La]_{b peak}. No significant differences in p¯ were observed between SL and ALT, for either 10 or 30 s ‘all out’ exercise; P_max during IE was significantly lower at ALT than at SL. [La]_{b peak} after 10 s ‘all out’ was unaffected by chronic hypoxia (7.0 ± 0.9 at ALT vs. 6.3 ± 1.8 mmol L^–1 at SL). After 30 s ‘all out’ the [La]_{b peak} decrease, at ALT (10.6 ± 0.6 mmol L^–1) vs. SL (12.9 ± 1.4 mmol L^–1), was only ～50% of that observed for IE (6.7 ± 1.6 mmol L^–1 vs. 11.3 ± 2.8 mmol L^–1). Muscle power output and blood lactate accumulation during short supramaximal exercise are substantially unaffected by chronic hypoxia.     

Cerebral oxygenation is reduced during hyperthermic exercise in humans

Aim: Cerebral mitochondrial oxygen tension (P_mitoO₂) is elevated during moderate exercise, while it is reduced when exercise becomes strenuous, reflecting an elevated cerebral metabolic rate for oxygen (CMRO₂) combined with hyperventilation-induced attenuation of cerebral blood flow (CBF). Heat stress challenges exercise capacity as expressed by increased rating of perceived exertion (RPE). Methods: This study evaluated the effect of heat stress during exercise on P_mitoO₂ calculated based on a Kety-Schmidt-determined CBF and the arterial-to-jugular venous oxygen differences in eight males [27 ± 6 years (mean ± SD) and maximal oxygen uptake (VO_2max) 63 ± 6 mL kg⁻¹ min⁻¹]. Results: The CBF, CMRO₂ and P_mitoO₂ remained stable during 1 h of moderate cycling (170 ± 11 W, ∼50% of VO_2max, RPE 9–12) in normothermia (core temperature of 37.8 ± 0.4 °C). In contrast, when hyperthermia was provoked by dressing the subjects in watertight clothing during exercise (core temperature 39.5 ± 0.2 °C), P_mitoO₂ declined by 4.8 ± 3.8 mmHg (P < 0.05 compared to normothermia) because CMRO₂ increased by 8 ± 7% at the same time as CBF was reduced by 15 ± 13% (P < 0.05). During exercise with heat stress, RPE increased to 19 (19–20; P < 0.05); the RPE correlated inversely with P_mitoO₂ (r² = 0.42, P < 0.05). Conclusion: These data indicate that strenuous exercise in the heat lowers cerebral P_mitoO₂, and that exercise capacity in this condition may be dependent on maintained cerebral oxygenation.     

High salt alone does not influence the kinetics of the Na+-H+antiporter

During a high-salt diet, tubular sodium reabsorption is decreased. This study concerns the effect of a high-salt diet on the proximal tubular (PT) Na⁺influx pathways. Brush-border membrane vesicles (BBMV) were prepared from rats on normal-salt (NS) and rats on high-salt (HS) diets. The initial uptake rates of Na⁺were the same in NS and HS rats, both in the absence and the presence of 1 mm amiloride. V_max and K_m for the amiloride-sensitive Na⁺/H⁺antiporter were also the same in the NS (V_max 3.69 ± 0.31 nmol mg prot^-110 s^-1, K_m 6.13 ± 0.58 mm ) and HS groups (V_max 3.54 ± 0.28 nmol mg prot^-110 s^-1, K_m 6.18 ± 0.64 mm ). There was no difference in the initial uptake rates of the Na⁺-glucose and the Na⁺-alanine symporters in NS and HS. V_max and K_m for the l -dopa-Na⁺symporter were also the same in NS (V_max 72 ± 2.5 pmol mg prot^-120 s^-1, K_m 98 ± 14 μm ) and HS groups (V_max 78 ± 6.0 pmol mg prot^-120 s^-1, K_m 106 ± 4 μm ). In summary, HS diet does not change the kinetics of the Na⁺transporters in the brush-border membrane of PT cells.     

Epidermal growth factor and insulin short‐term increase hPepT1‐mediated glycylsarcosine uptake in Caco‐2 cells

Aims: Little is known about the physiological regulation of the human intestinal di/tri‐peptide transporter, hPepT1. In the present study we evaluated the effects of epidermal growth factor (EGF) and insulin on hPepT1‐mediated dipeptide uptake in the intestinal cell line Caco‐2. Methods: Caco‐2 cells were grown on filters for 23–27 days. Apical dipeptide uptake was measured using [¹⁴C]glycylsarcosine([¹⁴C]Gly‐Sar). HPepT1 mRNA levels were investigated using RT‐PCR, cytosolic pH was determined using the pH‐sensitive fluorescent probe BCECF. Results: Basolateral application of EGF increased [¹⁴C]Gly‐Sar uptake with an ED₅₀ value of 0.77 ± 0.25 ng mL^?1 (n = 3?6) and a maximal stimulation of 33 ± 2% (n = 3?6). Insulin stimulated [¹⁴C]Gly‐Sar uptake with an ED₅₀ value of 3.5 ± 2.0 ng mL^?1 (n = 3?6) and a maximal stimulation of approximately 18% (n = 3?6). Gly‐Sar uptake followed simple Michaelis‐Menten kinetics. K_m in control cells was 0.98 ± 0.11 mM (n = 8) and V_max was 1.86 ± 0.07 nmol cm^?2 min^?1 (n = 8). In monolayers treated with 200 ng mL^?1 of EGF, K_m was 1.11 ± 0.05 mM (n = 5) and V_max was 2.79 ± 0.05 nmol cm^?2 min^?1 (n = 5). In monolayers treated with 50 ng mL^?1 insulin, K_m was 1.03 ± 0.08 mM and V_max was 2.19 ± 0.06 nmol cm^?2 min^?1 (n = 5). Kinetic data thus indicates an increase in the number of active transporters, following stimulation. The incrased Gly‐Sar uptake was not accompanied by changes in hPepT1 mRNA, nor by measurable changes in cytosolic pH. Conclusions: Short‐term stimulation with EGF and insulin caused an increase in hPepT1‐mediated uptake of Gly‐Sar in Caco‐2 cell monolayers, which could not be accounted for by changes in hPepT1 mRNA or proton‐motive driving force.     

Rate of oxidative phosphorylation in isolated mitochondria from human skeletal muscle: effect of training status

Muscle oxidative function has been investigated in subjects with various training status (VO _{2 max}, 41–72 mL O₂ kg^?1 body wt min^?1, n=10). Mitochondria were isolated from biopsies taken from m. vastus lateralis. Maximal mitochondrial oxygen consumption (QO ₂) and ATP production (MAPR) were measured with polarographic and bioluminometric techniques, respectively. The yield of mitochondria, calculated from the fractional activity of citrate synthase (CS), averaged 26%. With pyruvate + malate, the respiratory control ratio was 5.7 ± 0.4 (X ± SE) and the P/O ratio was 2.83 ± 0.02, which demonstrates that the isolated mitochondria were functionally intact. QO ₂ was significantly correlated to aerobic training status expressed as muscle CS activity (r=0.86), VO _{2 max} (r=0.84) and lactate threshold (r=0.83) but not to the fibre type composition. A highly significant correlation (r=0.93) was observed between ATP production calculated from QO ₂ and MAPR, but ATP production derived from QO ₂ was higher than MAPR both for pyruvate + malate (255%) and for α-ketoglutarate (23%). QO ₂ extrapolated to a temperature of 38 °C averaged 68 mL O₂ min^?1 kg^?1 wet wt, which is similar to previous findings in vitro and in vivo during the post-exercise period. However, calculated muscle O₂ utilization during exercise was three- to fivefold higher than QO ₂ measured on isolated mitochondria. It is suggested that additional factors exist for activation of mitochondrial respiration during exercise. It is concluded that muscle oxidative function can be quantitatively assessed from the respiration of mitochondria isolated from needle biopsy specimens and that QO ₂ is closely correlated to whole-body VO _{2 max}.     

Extracellular pH defense against lactic acid in untrained and trained altitude residents

The assumption that buffering at altitude is deteriorated by bicarbonate (bi) reduction was investigated. Extracellular pH defense against lactic acidosis was estimated from changes (Δ) in lactic acid ([La]), [HCO₃ ⁻], pH and PCO₂ in plasma, which equilibrates with interstitial fluid. These quantities were measured in earlobe blood during and after incremental bicycle exercise in 10 untrained (UT) and 11 endurance-trained (TR) highlanders (2,600 m). During exercise the capacity of non-bicarbonate buffers (β _nbi = −Δ[La] · ΔpH⁻¹ − Δ[HCO₃ ⁻] · ΔpH⁻¹) amounted to 40 ± 2 (SEM) and 28 ± 2 mmol l⁻¹ in UT and TR, respectively (P < 0.01). During recovery β _nbi decreased to 20 (UT) and 16 (TR) mmol l⁻¹ (P < 0.001) corresponding to values expected from hemoglobin, dissolved protein and phosphate concentrations related to extracellular fluid (ecf). This was accompanied by a larger decrease of base excess after than during exercise for a given Δ[La]. β _bi amounted to 37–41 mmol l⁻¹ being lower than at sea level. The large exercise β _nbi was mainly caused by increasing concentrations of buffers due to temporary shrinking of ecf. Tr has lower β _nbi in spite of an increased Hb mass mainly because of an expanded ecf compared to UT. In highlanders β _nbi is higher than in lowlanders because of larger Hb mass and reduced ecf and counteracts the decrease in [HCO₃ ⁻]. The amount of bicarbonate is probably reduced by reduction of the ecf at altitude but this is compensated by lower maximal [La] and more effective hyperventilation resulting in attenuated exercise acidosis at exhaustion.     

Similarity in physiological and perceived exertion responses to exercise at continuous and intermittent critical power

The purpose of this study was to compare the physiological responses [oxygen uptake (VO₂), heart rate (HR) and blood lactate concentrations ([BLa])] and the rating of perceived exertion (RPE) response until exhaustion (TTE) at the continuous (CP_c) and intermittent (CP_i) critical power workloads. Ten moderately active men (25.5 ± 4.2 years, 74.1 ± 8.0 kg, 177.6 ± 4.9 cm) participated in this study. The incremental test was applied to determine the highest values of oxygen uptake (VO_2max), heart rate (HR_max), blood lactate concentrations ([BLa_max]), and maximal aerobic power (MAP). Continuous and intermittent exhaustive predictive trials were performed randomly. The hyperbolic relation between power and time was used to estimate CP_c and CP_i. CP_i was derived from predictive trial results at an effort and recovery ratio of 30:30 s. Exercise at CP_c and CP_i as well as the physiological and RPE responses were measured until exhaustion. The values of physiological variables during CP_c and CP_i did not differ in either TTE test and were lower than the VO_2max, HR_max and [BLa_max] values. RPE was maximal at the end of exercise at CP_c and CP_i. There was a high correlation between VO_2max (L min⁻¹) and CP_c and CP_i intensities (r ≥ 0.90) and between MAP, CP_c and CP_i (r ≥ 0.95). Similar physiological and RPE responses were found at CP_c and CP_i for the times analyzed.     

Plasma catecholamine responses to four resistance exercise tests in men and women

The plasma adrenaline ([A]) and noradrenaline ([NA]) concentration responses of nine men and eight women were investigated in four resistance exercise tests (E80, E60, E40 and E20), in which the subjects had to perform a maximal number of bilateral knee extension-flexion movements at a given cycle pace of 0.5?Hz, but at different load levels (80%, 60%, 40% and 20% of 1 repetition maximum, respectively). The four test sessions were separated by a minimal interval of 3 rest days. The number of repetitions (Rep_max), the total work (W _tot) done normalized for the lean body mass and the heart rate (HR) responses were similar in the two groups in each test. In addition, no differences were found between the two groups in [A] and [NA] either before or after the exercise tests. The postexercise [NA], both in the men [10.8 (SD 7.0) nmol?·?l^?1] and in the women [11.7 (SD 7.4) nmol?·?l^?1], was clearly the highest in E20, where also the Rep_max, W _tot, the total amount of integrated electromyograph activity in the agonist muscles and the peak postexercise blood lactate concentration [men 8.3 (SD 1.6) vs women 7.3 (SD 0.9) mmol?·?l^?1, ns] were significantly higher than in the other tests. Although the postexercise [A] in E20 both in the men [7.1 (SD 6.0) nmol?·?l^?1] and in the women [5.2 (SD 2.0) nmol?·?l^?1] were higher than in E80 [men 3.1 (SD 4.2), women 2.1 (SD 2.0) nmol?·?l^?1] (P??1] and E40 [men 3.8 (SD 4.1), women 5.8 (SD 4.0) nmol?·?l^?1] in either group. The present study did not indicate any sex differences in performance and in plasma catecholamine responses in different exhausting resistance exercise tests performed with the knee extensor muscles. In both groups the plasma [NA] response was clearly the largest in the longest exercise with the greatest amount of muscle activity and work done, and with the largest blood lactate response. The differences in the plasma [A] responses between the exercises tended to be somewhat smaller.     

The relationship between monocarboxylate transporters 1 and 4 expression in skeletal muscle and endurance performance in athletes

The purpose of this study was to examine the relationship between skeletal muscle monocarboxylate transporters 1 and 4 (MCT1 and MCT4) expression, skeletal muscle oxidative capacity and endurance performance in trained cyclists. Ten well-trained cyclists (mean ± SD; age 24.4 ± 2.8 years, body mass 73.2 ± 8.3 kg, VO_2max 58 ± 7 ml kg⁻¹ min⁻¹) completed three endurance performance tasks [incremental exercise test to exhaustion, 2 and 10 min time trial (TT)]. In addition, a muscle biopsy sample from the vastus lateralis muscle was analysed for MCT1 and MCT4 expression levels together with the activity of citrate synthase (CS) and 3-hydroxyacyl-CoA dehydrogenase (HAD). There was a tendency for VO_2max and peak power output obtained in the incremental exercise test to be correlated with MCT1 (r = −0.71 to −0.74; P < 0.06), but not MCT4. The average power output (P _average) in the 2 min TT was significantly correlated with MCT4 (r = −0.74; P < 0.05) and HAD (r = −0.92; P < 0.01). The P _average in the 10 min TT was only correlated with CS activity (r = 0.68; P < 0.05). These results indicate the relationship between MCT1 and MCT4 as well as cycle TT performance may be influenced by the length and intensity of the task.     

Stroke volume response to cycle ergometry in trained and untrained older men

The aims of this study were threefold: (1) to investigate the stroke volume (SV) response of trained older male cyclists [Cyclists: 65 (2.1) years; n?=?10] during incremental cycle ergometry (20 W?·?min^?1); (2) to determine the SV dynamics and total peripheral resistance response of untrained, but healthy and active older male controls [Controls: 66 (1.1) years; n?=?10]; (3) to compare the maximum oxygen consumption (˙VO_2max) and SV response of trained older male runners [Runners: 65 (3.4) years; n?=?11] with that of age-matched Cyclists. Impedance cardiography was used to assess the response of cardiac output (CO), SV and total peripheral resistance to exercise involving cycle ergometry. The mean ˙VO_2max of the trained Cyclists [54 (1.6) ml?·?kg^?1?·?min^?1] was significantly higher (P??1?·?min^?1], whereas both groups possessed a significantly higher ˙VO_2max than the Controls [28 (1.3) ml?·?kg^?1?·?min^?1]. During exercise, at a heart rate of 90 beats?·?min^?1, the SV of the Cyclists increased by 41%, that of the Runners increased by 47%, and that of the Controls increased by 31%. However, the Cyclists' and Runners' SV response was significantly greater than that of the Controls. The SV for cyclists and controls peaked at 30% of ˙VO_2max. This early increase in SV was a major factor underlying the increase in CO during exercise in both the trained and the untrained subjects. In addition, all three groups showed a significant decrease in total peripheral resistance throughout exercise. The finding that older male runners possessed a large exercise SV and high ˙VO_2max suggests that run training results in enhanced cardiovascular performance during cycle ergometry.     

Correlation between heart rate and performance during Olympic windsurfing competition

The aim of this study was to examine the heart rate (HR) response to Olympic windsurfing competition and to check if there was any correlation between racing HR, performance, and the variables measured during laboratory maximal exercise. Ten elite windsurfers [age: 20.93 (3.46) years; height: 178.10 (6.34) cm; body mass: 66.79 (5.90) kg] performed a laboratory maximal oxygen consumption (VO_2max) trial and national windsurf competitions wearing a HR monitor. One hundred and forty-three individual races were examined. Racing HR was expressed as a percentage of (1) HR_max (maximal treadmill HR) and (2) HR_reserve (HR_max−HR_rest). The performance (racing classification: RC, which is inversely proportional to performance) was significantly correlated to the racing HR response in both light wind (LW): LW−RC=−0.12(%HR_reserve)+13.03; r=−0.71, r ²=0.50, p<0.001, and medium wind (MW): MW−RC=−0.11(%HR_reserve)+10.99; r=−0.66, r ²=0.43, p<0.001. The results showed similar correlations between performance and %HR_max. Post racing lactate concentration was higher in LW compared to MW [7.14 (0.21) and 5.18 (2.02) mmol·l⁻¹, respectively]. There was a negative correlation between the highest racing HR (%HR_reserve) of each athlete and the second ventilatory threshold expressed as a percentage of VO˙_2max (r=–0.71, p<0.05). To summarize, this study showed that light and medium wind Olympic windsurfing performances are highly dependent on the capacity of the athlete to maintain a high HR for long periods of time. Furthermore, windsurfing is highly dependent on the athlete's physical fitness level as shown by the correlations between racing HRs and laboratory physiological variables. Electronic Publication     

Choline transport and its osmotic regulation in renal cells derived from the rabbit outer medullary thick ascending limb of Henle

 Organic osmolytes such as betaine and glycerophosphorylcholine (GPC) are of major importance concerning volume regulation of inner and outer medullary epithelial cells. Recently we demonstrated that the intracellular betaine content in rabbit kidney cells derived from the outer medullary thick ascending limb of Henle’s loop (TALH) is osmotically regulated by betaine synthesis. In this context it was our purpose to characterize the uptake of choline, a precursor of betaine and GPC. We found TALH cells to possess a specific choline transport system with a maximum velocity (V _max) of 71 ± 12 pmol ·μl^–1 cell water · min^–1 and an apparent affinity (K _m) of 155 ± 19 μmol · l^–1. The uptake of choline was sodium independent and not electrogenic, but it was significantly reduced by the removement of chloride from the incubation medium. After long-term adaptation of TALH cells to a hyperosmotic medium (600 mosmol · l^–1, osmolarity adjusted with NaCl or urea) a significant higher choline uptake rate was observed (V _max: 166 ± 9 (NaCl), 96 ± 12 (urea) pmol ·μl^–1 cell water · min^–1). Our results suggest that the uptake of choline is due to higher intracellular requirements of choline under hypertonic conditions. Finally, an increase in the V _max of the choline transport system may enable sufficient synthesis of betaine and GPC. Received: 7 April 1997 / Received after revision: 2 June 1997 / Accepted: 3 June 1997     

Cardiovascular and ventilatory responses to electrically induced cycling with complete epidural anaesthesia in humans

Cardiovascular and ventilatory responses to electrically induced dynamic exercise were investigated in eight healthy young males with afferent neural influence from the legs blocked by epidural anaesthesia (25 ml 2% lidocaine) at L3-L4. This caused cutaneous sensory anaesthesia below T8-T9 and complete paralysis of the legs. Cycling was performed for 22.7 ± 2.7 min (mean, SE) (fatigue) and oxygen uptake (Vo₂) increased to 1.90 ± 0.13 1 min^-1. Compared with voluntary exercise at the same Vo₂, increases in heart rate (HR) (135 ± 7 vs. 130 ± 9 beats min^-1) and cardiac output (16.9 ± 1.1 vs. 17.3 ± 0.9 1 min^-1) were similar, and ventilation (54 ± 5 vs. 45 ± 4 1 min^-1) was higher (P < 0.05). In contrast, the rise in mean arterial blood pressure during voluntary exercise (93 ± 4 (rest) to 119 ± 4 mmHg (exercise)) was not manifest during electrically induced exercise with epidural anaesthesia [93 ± 3 (rest) to 95 ± 5 mmHg (exercise)]. As there is ample evidence for similar cardiovascular and ventilatory responses to electrically induced and voluntary exercise (Strange et al. 1993), the present results support the fact that the neural input from working muscle is crucial for the normal blood pressure response to exercise. Other haemodynamic and/or humoral mechanisms must operate in a decisive manner in the control of HR, CO and VE during dynamic exercise with large muscle groups.